Several previous studies have shown that .gamma.-aminobutyric acid is a major inhibitory transmitter of the central nervous system as reported, for example, by Y. Godin et al., Journal Neurochemistry, 16, 869 (1969) and that disturbance of the excitation and inhibition interplay can lead to diseased states such as Huntington's chorea (The Lancet, Nov. 9, 1974, pp. 1122-1123) Parkinsonism, schizophrenia, epilepsy, depression, hyperkinesis and manic depression disorders, Biochem. Pharmacol. 23, 2637-2649 (1974). Certain compounds are known to elevate brain levels of .gamma.-aminobutyric acid, for example, n-dipropylacetate [Simler et al., Biochem. Pharm., 22, 1701 (1973)] by competitively inhibiting .gamma.-aminobutyric acid transaminase resulting in a reversible effect which lasts for only about 2 hours. Also, 4-aminotetrolic acid [P. M. Beart et al., J. Neurochem. 19, 1849 (1972)] is known to be a competitive reversible inhibitor of .gamma.-aminobutyric acid transaminase. We have now made the unexpected finding that compounds of our invention are able to irreversibly inhibit .gamma.-aminobutyric acid transaminase and increase significantly the brain level of .gamma.-aminobutyric acid in animals, rendering them useful in the treatment of the aforementioned diseased states. Furthermore, this increase is long lasting (over 24 hours) and, therefore, compounds of the present invention are not only structurally novel but are quite different in their properties from known compounds which elevate brain levels of .gamma.-aminobutyric acid only for a short period of time.